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在运动神经元中诱导依赖氧化的亡,由缺乏的超氧化物脱酶诱导.

A G Estévez¹, J P Crow, J B Sampson

¹Department of Anesthesiology, University of Alabama at Birmingham, Birmingham, AL 35233, USA.

Science (New York, N.Y.)

|January 5, 2000

概括

此摘要是机器生成的。

在铜中缺,超氧化物脱酶 (SOD) 导致肌缩性侧面硬化症 (ALS) 中的运动神经元死亡. 这种毒性涉及氧化和铜结合,突出SOD.

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科学领域:

神经科学是一个神经科学.
生物化学生物化学
遗传学是一个遗传学.

背景情况:

铜,超氧化物脱酶 (SOD) 中的突变与某种类型的肌缩性侧面硬化症 (ALS) 病例中的运动神经元退化有关.
蛋白质SOD对抗氧化应激的细胞防御至关重要,存在各种形式,包括在ALS患者中发现的野生类型和突变变异型.